Sunday, May 01, 2016

Bacterial translocation peri cardiac arrest

During
the periarrest period, intestinal ischemia may result in barrier
dysfunction and bacterial translocation, which has clear mechanistic
links to inflammation and cascade stimulation, especially in patients
who are treated with therapeutic hypothermia. Despite optimal
management, periarrest bacterial translocation may worsen the outcome
of cardiac arrest victims.

But
the relationship between infection and cardiac arrest is more complex
than we might imagine. Emerging evidence is beginning to suggest
that antibiotics may be indicated in non-shockable out of hospital
cardiac arrest. From the body of the paper:

One
of the main goals both during CPR and postresuscitation period is
hemodynamic optimization to preserve adequate coronary and cerebral
perfusion. However, intestinal ischemia, a neglected consequence of
circulatory collapse, and subsequent reperfusion may be extremely
detrimental by enhancing bacterial translocation [3] . This
phenomenon is likely more common in patients presenting with asystole
or pulseless electrical activity (PEA) rather than ventricular
fibrillation or pulseless ventricular tachycardia due to the
prolongation of whole-body ischemia in nonshockable cardiac arrest.
Asystole has been reported as the most common presenting rhythm in
OHCA victims with bacteremia followed by PEA and ventricular
fibrillation [4] , whereas, in a retrospective analysis, shockable
rhythms were uncommon among patients with preexisting pneumonia
compared with initial arrest rhythms in patients without pneumonia
[5] . Although the initial rhythm in OHCA is rarely recorded and may
have evolved to asystole at the time of the recording, we have also
reported PEA as the initial cardiac arrest rhythm in severe sepsis
and septic shock [6] .

Research
so far has shown that more than one third of OHCA victims are
bacteremic upon presentation [4] ; however, it is difficult to know
if sepsis is the reason for cardiac arrest or bacteremia is a
downstream effect of intestinal hypoperfusion.

Multiple
purported mechanisms are discussed including the use of saline as
resuscitation fluid and the use of therapeutic hypothermia.